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Recruitment of the mitochondrial-dependent apoptotic pathway in amyotrophic lateral sclerosis
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Limongi et al recently showed that a GSH derivate (N-butanoyl glutathione, GSH-C4) is able to penetrate cell membranes and buffer GSH depletion, thus counteract on the pro-inflammatory response in different cellular models of inflammation, by reducing the expression of pro-inflammatory cytokines via NFkB modulation